The effect of three rad genes on survival, inter- and intragenic mitotic recombination in Saccharomyces

1975 ◽  
Vol 136 (1) ◽  
pp. 75-86 ◽  
Author(s):  
Susanne Kowalski ◽  
Wolfgang Laskowski
Keyword(s):  
Mitotic Recombination ◽  
Rad Genes

scholarly journals RELATIONSHIPS BETWEEN A HYPER-REC MUTATION (rem1) AND OTHER RECOMBINATION AND REPAIR GENES IN YEAST

Genetics ◽  
1984 ◽  
Vol 107 (1) ◽  
pp. 33-48
Author(s):  
Robert E Malone ◽  
Merl F Hoekstra
Keyword(s):  
Meiotic Recombination ◽  
Mitotic Recombination ◽  
Repair System ◽  
X Rays ◽  
Recombination System ◽  
Damage Repair ◽  
Rad6 Gene ◽  
Recombination Repair ◽  
Rad Genes ◽  
Repair Genes

ABSTRACT Mutations in the REM1 gene of Saccharomyces cerevisiae confer a semidominant hyper-recombination and hypermutable phenotype upon mitotic cells (Golin and Esposito 1977). These effects have not been observed in meiosis. We have examined the interactions of rem1 mutations with rad6-1, rad50-1, rad52-1 or spo11-1 mutations in order to understand the basis of the rem1 hyper-rec phenotype. The rad mutations have pleiotropic phenotypes; spo11 is only defective in sporulation and meiosis. The RAD6, RAD50 and SPO11 genes are not required for spontaneous mitotic recombination; mutations in the RAD52 gene cause a general spontaneous mitotic Rec- phenotype. Mutations in RAD50, RAD52 or SPO11 eliminate meiotic recombination, and mutations in RAD6 prevent spore formation. Evidence for the involvement of RAD6 in meiotic recombination is less clear. Mutations in all three RAD genes confer sensitivity to X rays; the RAD6 gene is also required for UV damage repair. To test whether any of these functions might be involved in the hyper-rec phenotype conferred by rem1 mutations, double mutants were constructed. Double mutants of rem1 spo11 were viable and demonstrated rem1 levels of mitotic recombination, suggesting that the normal meiotic recombination system is not involved in producing the rem1 phenotype. The rem1 rad6 double mutant was also viable and had rem1 levels of mitotic recombination. Neither rem1 rad50 nor rem1 rad52 double mutants were viable. This suggests that rem1 causes its hyper-rec phenotype because it creates lesions in the DNA that are repaired using a recombination-repair system involving RAD50 and RAD52.

scholarly journals A New Hyperrecombination Mutation Identifies a Novel Yeast Gene, THP1, Connecting Transcription Elongation With Mitotic Recombination

Genetics ◽  
2001 ◽  
Vol 157 (1) ◽  
pp. 79-89 ◽  
Author(s):  
Mercedes Gallardo ◽  
Andrés Aguilera
Keyword(s):  
Genomic Instability ◽  
Dna Sequences ◽  
Unknown Function ◽  
Genetic Instability ◽  
Transcription Elongation ◽  
Mitotic Recombination ◽  
Yeast Gene ◽  
Transcription Terminator ◽  
New Gene ◽  
New Evidence

Abstract Given the importance of the incidence of recombination in genomic instability, it is of great interest to know the elements or processes controlling recombination in mitosis. One such process is transcription, which has been shown to induce recombination in bacteria, yeast, and mammals. To further investigate the genetic control of the incidence of recombination and genetic instability and, in particular, its connection with transcription, we have undertaken a search for hyperrecombination mutants among a large number of strains deleted in genes of unknown function. We have identified a new gene, THP1 (YOL072w), whose deletion mutation strongly stimulates recombination between repeats. In addition, thp1Δ impairs transcription, a defect that is particularly strong at the level of elongation through particular DNA sequences such as lacZ. The hyperrecombination phenotype of thp1Δ cells is fully dependent on transcription elongation of the repeat construct. When transcription is impeded either by shutting off the promoter or by using a premature transcription terminator, hyperrecombination between repeats is abolished, providing new evidence that transcription-elongation impairment may be a source of recombinogenic substrates in mitosis. We show that Thp1p and two other proteins previously shown to control transcription-associated recombination, Hpr1p and Tho2p, act in the same “pathway” connecting transcription elongation with the incidence of mitotic recombination.

scholarly journals A 160-bp Palindrome Is a Rad50·Rad32-Dependent Mitotic Recombination Hotspot inSchizosaccharomyces pombe

Genetics ◽  
2002 ◽  
Vol 161 (1) ◽  
pp. 461-468 ◽  
Author(s):  
Joseph A Farah ◽  
Edgar Hartsuiker ◽  
Ken-ichi Mizuno ◽  
Kunihiro Ohta ◽  
Gerald R Smith
Keyword(s):  
Secondary Structure ◽  
Schizosaccharomyces Pombe ◽  
Inverted Repeat ◽  
Mitotic Recombination ◽  
Genome Integrity ◽  
Recombination Hotspot ◽  
Nuclease Domain ◽  
Palindromic Sequences

AbstractPalindromic sequences can form hairpin and cruciform structures that pose a threat to genome integrity. We found that a 160-bp palindrome (an inverted repeat of 80 bp) conferred a mitotic recombination hotspot relative to a control nonpalindromic sequence when inserted into the ade6 gene of Schizosaccharomyces pombe. The hotspot activity of the palindrome, but not the basal level of recombination, was abolished by a rad50 deletion, by a rad50S “separation of function” mutation, or by a rad32-D25A mutation in the nuclease domain of the Rad32 protein, an Mre11 homolog. We propose that upon extrusion of the palindrome the Rad50·Rad32 nuclease complex recognizes and cleaves the secondary structure thus formed and generates a recombinogenic break in the DNA.

scholarly journals Regulation of Mitotic Homeologous Recombination in Yeast: Functions of Mismatch Repair and Nucleotide Excision Repair Genes

Genetics ◽  
2000 ◽  
Vol 154 (1) ◽  
pp. 133-146 ◽  
Author(s):  
Ainsley Nicholson ◽  
Miyono Hendrix ◽  
Sue Jinks-Robertson ◽  
Gray F Crouse
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mismatch Repair ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Mitotic Recombination ◽  
Inverted Repeats ◽  
Replication Errors ◽  
Nucleotide Excision ◽  
Homeologous Recombination ◽  
Repair Genes

Abstract The Saccharomyces cerevisiae homologs of the bacterial mismatch repair proteins MutS and MutL correct replication errors and prevent recombination between homeologous (nonidentical) sequences. Previously, we demonstrated that Msh2p, Msh3p, and Pms1p regulate recombination between 91% identical inverted repeats, and here use the same substrates to show that Mlh1p and Msh6p have important antirecombination roles. In addition, substrates containing defined types of mismatches (base-base mismatches; 1-, 4-, or 12-nt insertion/deletion loops; or 18-nt palindromes) were used to examine recognition of these mismatches in mitotic recombination intermediates. Msh2p was required for recognition of all types of mismatches, whereas Msh6p recognized only base-base mismatches and 1-nt insertion/deletion loops. Msh3p was involved in recognition of the palindrome and all loops, but also had an unexpected antirecombination role when the potential heteroduplex contained only base-base mismatches. In contrast to their similar antimutator roles, Pms1p consistently inhibited recombination to a lesser degree than did Msh2p. In addition to the yeast MutS and MutL homologs, the exonuclease Exo1p and the nucleotide excision repair proteins Rad1p and Rad10p were found to have roles in inhibiting recombination between mismatched substrates.

scholarly journals ALTERED FIDELITY OF MITOTIC CHROMOSOME TRANSMISSION IN CELL CYCLE MUTANTS OF S. CEREVISIAE

Genetics ◽  
1985 ◽  
Vol 110 (3) ◽  
pp. 381-395
Author(s):  
Leland H Hartwell ◽  
David Smith
Keyword(s):  
Cell Cycle ◽  
Gene Product ◽  
Mitotic Chromosome ◽  
Mitotic Recombination ◽  
Chromosome Loss ◽  
Temperature Sensitive ◽  
Repair Pathway ◽  
Dna Metabolism ◽  
Temperature Sensitive Mutants ◽  
Chromosome Transmission

ABSTRACT Thirteen of 14 temperature-sensitive mutants deficient in successive steps of mitotic chromosome transmission (cdc2, 4, 5, 6, 7, 8, 9, 13, 14, 15, 16, 17 and 20) from spindle pole body separation to a late stage of nuclear division exhibited a dramatic increase in the frequency of chromosome loss and/or mitotic recombination when they were grown at their maximum permissive temperatures. The increase in chromosome loss and/or recombination is likely to be due to the deficiency of functional gene product rather than to an aberrant function of the mutant gene product since the mutant alleles are, with one exception, recessive to the wild-type allele for this phenotype. The generality of this result suggests that a delay in almost any stage of chromosome replication or segregation leads to a decrease in the fidelity of mitotic chromosome transmission. In contrast, temperature-sensitive mutants defective in the control step of the cell cycle (cdc28), in cytokinesis (cdc3) or in protein synthesis (ils1) did not exhibit increased recombination or chromosome loss.—Based upon previous results with mutants and DNA-damaging agents in a variety of organisms, we suggest that the induction of mitotic recombination in certain mutants is due to the action of a repair pathway upon nicks or gaps left in the DNA. This interpretation is supported by the fact that the induced recombination is dependent upon the RAD52 gene product, an essential component in the recombinogenic DNA repair pathway. Gene products whose deficiency leads to induced recombination are, therefore, strong candidates for proteins that function in DNA metabolism. Among the mutants that induce recombination are those known to be defective in some aspect of DNA replication (cdc2, 6, 8, 9) as well as some mutants defective in the G2 (cdc13 and 17) and M (cdc5 and 14) phases of the mitotic cycle. We suggest that special aspects of DNA metabolism may be occurring in G2 and M in order to prepare the chromosomes for proper segregation.

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